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Effects of N-acetylcysteine on Low T3 Syndrome

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ClinicalTrials.gov Identifier: NCT01501110
Recruitment Status : Completed
First Posted : December 29, 2011
Results First Posted : March 31, 2015
Last Update Posted : March 31, 2015
Information provided by (Responsible Party):

November 25, 2011
December 29, 2011
December 3, 2014
March 31, 2015
March 31, 2015
November 2011
July 2013   (Final data collection date for primary outcome measure)
Serum T3 Levels at 48 Hours [ Time Frame: 48 hours ]
Change from baseline in serum T3 levels at 48 hours [ Time Frame: baseline and 48 hours ]
Complete list of historical versions of study NCT01501110 on ClinicalTrials.gov Archive Site
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Effects of N-acetylcysteine on Low T3 Syndrome
Evaluation of the Effects of N-acetylcysteine on Thyroid Hormone Levels in the Low T3 Syndrome
The propose of this study is to determine whether N-acetylcysteine is effective in reversing the changes in thyroid hormones seen in critical illness, known as the low T3 syndrome.

The low T3 syndrome or nonthyroidal illness is characterized by low levels of T3, normal or high normal levels of rT3, low or normal levels of T4 and inappropriately normal or low levels of TSH. These changes affect up to 75% of patients and have prognostic implications.

Interleukin-6 (IL6) seems to have a causative role in the pathogenesis of nonthyroidal illness. There is evidence that the reduction in serum T3 was inversely associated with serum IL-6, while the rT3 have a positive association. The mechanism of action of cytokines on the metabolism of thyroid hormones has not been determined and the potential role of cytokines on the deiodases has been the focus of research.

In a cell culture model study, IL-6 was able to suppress the conversion of T4 to T3 by deiodases type 1 and 2 and stimulate the inactivation of T3 by deiodase type 3, a situation similar to nonthyroidal illness. The use of N-acetylcysteine prevented this alterations, been consistent with the hypothesis that IL6 inhibits the function of the deiodases by increasing the oxygen reactive species and by consuming gluthathione or some gluthathione dependent cofactor.

Considering the absence of human studies evaluating the use of N-acetylcysteine in nonthyroidal illness, the aim of this study is to investigate whether NAC has in vivo effect on changes of thyroid hormones.

Phase 4
Allocation: Randomized
Intervention Model: Parallel Assignment
Masking: Single (Participant)
Primary Purpose: Treatment
  • Acute Myocardial Infarction
  • Euthyroid Sick Syndrome
  • Ischemic Heart Disease
Drug: N-acetylcysteine
in infusion of 1200 mg of n-acetylcysteine twice a day for 48 hours
Other Names:
  • NAC
  • acetylcysteine
  • Active Comparator: n-acetylcysteine
    intra-venous infusion of 1200 mg of n-acetylcysteine twice a day for 48 hours.
    Intervention: Drug: N-acetylcysteine
  • No Intervention: no intervention
    No intervention

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
November 2013
July 2013   (Final data collection date for primary outcome measure)

Inclusion Criteria:

  • diagnosis of acute myocardial infarction with less than 12 hours of evolution
  • reperfusion therapy (primary angioplasty)

Exclusion Criteria:

  • Thyroid disease
  • Chronic renal disease with renal replacement therapy
  • hepatic insufficiency
  • immunosuppression
Sexes Eligible for Study: All
18 Years to 80 Years   (Adult, Senior)
Contact information is only displayed when the study is recruiting subjects
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Josi Vidart, Federal University of Rio Grande do Sul
Federal University of Rio Grande do Sul
  • Hospital de Clinicas de Porto Alegre
  • Programa de pós-graduação em endocrinologia
Principal Investigator: Josi Vidart Federal University of Rio Grande do Sul
Study Director: Ana maia Federal University of Rio Grande do Sul
Federal University of Rio Grande do Sul
March 2015

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP